ArticleThe Journal of investigative dermatology2015
Promoter-Specific Hypomethylation Is Associated with Overexpression of PLS3, GATA6, and TWIST1 in the Sezary Syndrome.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Epigenetic regulation of plastin 3 expression by the macrosatellite DXZ4 and the transcriptional regulator CHD4.American journal of human genetics · 2023Article
- An "unexpected" role for EMT transcription factors in hematological development and malignancy.Frontiers in immunology · 2023Review
- Single-cell analyses reveal novel molecular signatures and pathogenesis in cutaneous T cell lymphoma.Cell death & disease · 2022Article
- Epigenetics of Cutaneous T-Cell Lymphomas.International journal of molecular sciences · 2022Review
- Review
- Cutaneous T cell lymphoma.Nature reviews. Disease primers · 2021Review
- Plastin 3 in health and disease: a matter of balance.Cellular and molecular life sciences : CMLS · 2021Review
- Normal and cancer fibroblasts differentially regulate TWIST1, TOX and cytokine gene expression in cutaneous T-cell lymphoma.BMC cancer · 2021Article
- Epigenetics of cutaneous T-cell lymphoma: biomarkers and therapeutic potentials.Cancer biology & medicine · 2021Review
- Epigenetics in the Pathogenesis and Treatment of Cutaneous T-Cell Lymphoma.Frontiers in oncology · 2021Review
- Hypomethylation of the promoter region drives ectopic expression of TMEM244 in Sézary cells.Journal of cellular and molecular medicine · 2020Article
- Review
- Purity estimation from differentially methylated sites using Illumina Infinium methylation microarray data.Cell cycle (Georgetown, Tex.) · 2020Article
- Twist-1 is upregulated by NSD2 and contributes to tumour dissemination and an epithelial-mesenchymal transition-like gene expression signature in t(4;14)-positive multiple myeloma.Cancer letters · 2020Article
- Transcriptome analysis of Sézary syndrome and lymphocytic-variant hypereosinophilic syndrome T cells reveals common and divergent genes.Oncotarget · 2019Article
- Article
- A study of meiomitosis and novel pathways of genomic instability in cutaneous T-cell lymphomas (CTCL).Oncotarget · 2018Article
- Emerging roles of epithelial-mesenchymal transition in hematological malignancies.Journal of biomedical science · 2018Review
- EMT- and MET-related processes in nonepithelial tumors: importance for disease progression, prognosis, and therapeutic opportunities.Molecular oncology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The Sézary Syndrome (SS) is an aggressive CD4+ leukemic variant of cutaneous T-cell lymphoma. Epigenetic modification of cancer cell genome is often linked to the expression of important cancer-related genes. Here we addressed the hypothesis that, in SS, DNA hypomethylation is involved in upregulation of PLS3, GATA6, and TWIST1, genes that are undetected in normal lymphocytes. Pyrosequencing analysis of CpG rich regions, and CpG dinucleotides within the 5' regulatory regions, confirmed hypomethylation of all three genes in SS, compared with controls. We then studied how methylation regulates PLS3 transcription in vitro using PLS3-negative (Jurkat) and PLS3-positive (HT-1080) cell lines. Treatment with the hypomethylating agent 5-azacytidine induced PLS3 expression in Jurkat cells and in vitro methylation of the cloned PLS3 promoter suppressed luciferase expression in HT-1080 cells. In conclusion, we show that promoter hypomethylation is associated with PLS3, GATA6, and TWIST1 overexpression in SS CD4+ T cells and that methylation can regulate PLS3 expression in vitro. The mechanisms of DNA hypomethylation in vivo and the functional role of PLS3, TWIST1, and GATA6 in SS are being investigated.
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Registered trials
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